Researchers discover anti-ageing function of human cell protein which helps repair damaged mitochondria

Researchers have found an anti-ageing function in a protein deep within human cells. The protein, ATSF-1, controlled the fine balance between creation of new and repair of damaged mitochondria, the part of cell responsible for producing energy, the researchers at the Queensland Brain Institute (QBI), The University of Queensland, Australia, discovered.

"Mitochondrial dysfunction lies at the core of many human diseases, including common age-related diseases such as dementias and Parkinson's," said associate professor at QBI, Steven Zuryn.

While the energy produced by the mitochondria powers biological functions, the toxic by-products of this process contribute to the ageing process of the cell.


"Our finding could have exciting implications for healthy ageing and for people with inherited mitochondrial diseases.

"In conditions of stress, when mitochondrial DNA has been damaged, the ATSF-1 protein prioritises repair which promotes cellular health and longevity," said Zuryn.

As an analogy, Zuryn likened the relationship to a race car needing a pitstop.

"ATSF-1 makes the call that a pitstop is needed for the cell when mitochondria need repairs.

"We studied ATFS-1 in C. elegans, or round worms, and saw that enhancing its function promoted cellular health, meaning the worms became more agile for longer.

"They didn't live longer, but they were healthier as they aged," said Zuryn.

Understanding how cells promote repair is an important step towards identifying possible interventions to prevent mitochondrial damage, the authors said in the study published in the journal Nature Cell Biology said.

"Our goal is to prolong the tissue and organ functions that typically decline during ageing by understanding how deteriorating mitochondria contribute to this process," said Michael Dai, QBI.

"We may ultimately design interventions that keep mitochondrial DNA healthier for longer, improving our quality of life," said Dai.